Amphotericin B blunts erythropoietin response to anemia.
Amphotericin B causes a normochromic, normocytic anemia thought to be mediated by direct marrow toxicity or suppression of erythropoietin production. Serial hemoglobin, hematocrit, amphotericin B, and erythropoietin levels were determined before, during, and after completion of amphotericin B therapy for three patients without significant renal disease or active hematologic malignancy. Patients with systemic fungal diseases treated with itraconazole served as controls. Serum erythropoietin levels were determined by radioimmunoassay and amphotericin B by high-performance liquid chromatography. Despite anemia in all amphotericin B-treated patients, erythropoietin levels declined or remained relatively constant during therapy while erythropoietin levels in controls were appropriate for the degree of anemia. Within 2 weeks of completion of amphotericin B treatment, two patients had increasing erythropoietin levels in response to anemia. Amphotericin B appears to suppress but not abolish the erythropoietin response to anemia; this effect disappears quickly after discontinuation of the drug.
Lin
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AC
Department of Medicine, University of Mississippi Medical Center, Jackson 39216-4505.
Goldwasser
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E
Bernard
E M
EM
Chapman
S W
SW
D000666:Amphotericin B / Q000009:adverse effects* / Q000097:blood; D000740:Anemia / Q000097:blood / Q000139:chemically induced*; D002851:Chromatography, High Pressure Liquid; D003404:Creatinine / Q000097:blood; D004921:Erythropoietin / Q000096:biosynthesis* / Q000097:blood; D006400:Hematocrit; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D011863:Radioimmunoassay
D006454:Hemoglobins; D004921:Erythropoietin; D000666:Amphotericin B; D003404:Creatinine